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. 2021 Feb 11;13(2):277. doi: 10.3390/v13020277

Figure 2.

Figure 2

Human Exogenous and Endogenous RVs initiate proinflammatory intracellular pathways converging on critical immune genes involved in SLE pathogenesis. Exogenous RVs RNA and retrotranscribed DNA can activate different cellular sensors located at plasmatic (1) and endosomal membranes (2) or in the cytosol (3), triggering a proinflammatory response (Panel A). HERVs similarly activate endosomal TLRs and also mediate the effects of environmental factors on critical immune genes: estrogens, UVB and infections can increase HERV-E clone 4-1 mRNA expression in SLE CD4+ T-cells and PBMCs, activating a cascade which leads to DNA hypomethylation and type I IFN response (Panel B). Legend: MyD88: Myeloid differentiation primary response 88, TRIF: TIR-domain-containing adapter-inducing interferon-β, TRAM: TRIF-related adaptor molecule, AP-1: activator protein-1, cGAS: cyclic GMP-AMP synthase, cGAMP: cyclic guanosine monophosphate-adenosine monophosphate, STING: cyclic GMP-AMP receptor stimulator of interferon genes, TBK: TANK-binding kinase, IRF: interferon regulator factor, RIG-1: retinoic acid-inducible gene 1, MDA5: melanoma differentiation-associated protein-5, AIM2: absent in melanoma 2, DAI: DNA-dependent activator of interferon regulatory factor, IFI16: γ-interferon-inducible protein IFI-16, MAVS: mitochondrial antiviral signaling protein, LGP2: the laboratory of genetics and physiology 2, NFAT1: nuclear factor of activated T cells 1, MBD2: methyl-CpG-binding domain protein 2,UVB: ultraviolet beams, ERα: estrogen receptor alpha.